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EBNA3A contributes to the regulation of p16INK4A.

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posted on 10.06.2010, 01:55 by Lenka Skalska, Robert E. White, Melanie Franz, Michaela Ruhmann, Martin J. Allday

(A) Western blot analysis of three LCLs established with virus derived from B95.8-EBV BAC (WT) and two established with EBNA3A-KO recombinants. The steady state levels of p16INK4A (p16) are elevated in the EBNA3A-KO cells relative to the WT-EBV infected cells. It should be noted that similar results were reported using a larger panel of EBNA3A-KO LCLs [8]. An LCL 3CHT (3CHT) with (+) or without (-) HT is shown for comparison. (B) & (C) ChIP analysis of H3K27me3 and H3K4me3 distribution on exon 1 (site C) and site A in the p16INK4A-ARF locus from an EBNA3A-KO LCL (3AKO) and a WT-EBV LCL (WT).